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GWAS Study

Whole-Exome Sequencing Study Identifies Four Novel Gene Loci Associated with Diabetic Kidney Disease.

Pan Y, Sun X, Mi X et al.

36444934 PubMed ID
GWAS Study Type
10762 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

PY
Pan Y
SX
Sun X
MX
Mi X
HZ
Huang Z
HY
Hsu Y
HJ
Hixson JE
MD
Munzy D
MG
Metcalf G
FN
Franceschini N
TA
Tin A
KA
Köttgen A
FM
Francis M
BJ
Brody JA
KB
Kestenbaum B
SC
Sitlani CM
MJ
Mychaleckyj JC
KH
Kramer H
LL
Lange LA
GX
Guo X
HS
Hwang SJ
IM
Irvin MR
SJ
Smith JA
YL
Yanek LR
VD
Vaidya D
CY
Chen YI
FM
Fornage M
LD
Lloyd-Jones DM
HL
Hou L
MR
Mathias RA
MB
Mitchell BD
PP
Peyser PA
KS
Kardia SLR
AD
Arnett DK
CA
Correa A
RL
Raffield LM
VR
Vasan RS
CL
Cupple LA
LD
Levy D
KR
Kaplan RC
NK
North KE
RJ
Rotter JI
KC
Kooperberg C
RA
Reiner AP
PB
Psaty BM
TR
Tracy RP
GR
Gibbs RA
MA
Morrison AC
FH
Feldman H
BE
Boerwinkle E
HJ
He J
KT
Kelly TN
Chapter II

Abstract

Summary of the research findings

Diabetic kidney disease (DKD) is recognized as an important public health challenge. However, its genomic mechanisms are poorly understood. To identify rare variants for DKD, we conducted a whole-exome sequencing (WES) study leveraging large cohorts well-phenotyped for chronic kidney disease and diabetes. Our two-stage WES study included 4372 European and African ancestry participants from the Chronic Renal Insufficiency Cohort and Atherosclerosis Risk in Communities studies (stage 1) and 11 487 multi-ancestry Trans-Omics for Precision Medicine participants (stage 2). Generalized linear mixed models, which accounted for genetic relatedness and adjusted for age, sex and ancestry, were used to test associations between single variants and DKD. Gene-based aggregate rare variant analyses were conducted using an optimized sequence kernel association test implemented within our mixed model framework. We identified four novel exome-wide significant DKD-related loci through initiating diabetes. In single-variant analyses, participants carrying a rare, in-frame insertion in the DIS3L2 gene (rs141560952) exhibited a 193-fold increased odds [95% confidence interval (CI): 33.6, 1105] of DKD compared with noncarriers (P = 3.59 × 10-9). Likewise, each copy of a low-frequency KRT6B splice-site variant (rs425827) conferred a 5.31-fold higher odds (95% CI: 3.06, 9.21) of DKD (P = 2.72 × 10-9). Aggregate gene-based analyses further identified ERAP2 (P = 4.03 × 10-8) and NPEPPS (P = 1.51 × 10-7), which are both expressed in the kidney and implicated in renin-angiotensin-aldosterone system modulated immune response. In the largest WES study of DKD, we identified novel rare variant loci attaining exome-wide significance. These findings provide new insights into the molecular mechanisms underlying DKD.

296 European ancestry cases, 1,660 European ancestry controls, 297 African or African American cases, 406 African or African American controls

Chapter III

Study Statistics

Key metrics and study information

10762
Total Participants
GWAS
Study Type
Yes
Replicated
154 Hispanic/Latino or Asian ancestry cases, 888 Hispanic/Latino or Asian ancestry controls, 265 African or African American cases, 1,738 African or African American controls, 182 European ancestry cases, 4,876 European ancestry controls
Replication Participants
European, African unspecified, African American or Afro-Caribbean, Hispanic or Latin American, East Asian, Asian unspecified
Ancestry
U.S., China
Recruitment Country
Chapter IV

Analysis

Comprehensive review of health and genetic findings

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